The Experts below are selected from a list of 186 Experts worldwide ranked by ideXlab platform

Shamgar Beneliyahu - One of the best experts on this subject based on the ideXlab platform.

  • male female differences in the impact of β adrenoceptor stimulation on resistance to experimental metastasis exploring the effects of age and gonadal hormone involvement
    Journal of Neuroimmunology, 2008
    Co-Authors: Gayle G Page, Andrea M Fennelly, Marguerite T Littletonkearney, Shamgar Beneliyahu
    Abstract:

    We studied the development of sexual dimorphism in resistance to NK-sensitive experimental metastasis under baseline conditions and following adrenoceptor stimulation. With increasing age, baseline resistance to MADB106 lung tumor retention (LTR) increased in both sexes, but also the susceptibility to the tumor-enhancing effects of a β-adrenergic agonist, Metaproterenol. Beginning at 13 weeks, males exhibited a 2- to 3-fold greater increase in LTR than females following adrenoceptor stimulation. This adult dimorphism was robust to ovariectomy, and questionably related to androgens. The findings are consistent with reduced female responsiveness to sympathetic activation, and substantiate the importance of including both sexes when studying neuroimmunomodulation.

  • marginating pulmonary nk activity and resistance to experimental tumor metastasis suppression by surgery and the prophylactic use of a β adrenergic antagonist and a prostaglandin synthesis inhibitor
    Brain Behavior and Immunity, 2005
    Co-Authors: Rivka Melamed, Ella Rosenne, Keren Shakhar, Yossi Schwartz, Naphtali Abudarham, Shamgar Beneliyahu
    Abstract:

    Surgery is imperative for cancer treatment, but was suggested to suppress immunity and facilitate metastasis. Here we study the involvement of catecholamines and prostaglandins (PG) in such outcomes, and the role played by marginating-pulmonary (MP)-NK cells in controlling MADB106 metastasis. Non-operated and laparotomized F344 rats were injected postoperatively with a PG synthesis inhibitor (indomethacin, 4 mg/kg i.p.), a beta-blocker (nadolol, 0.6 mg/kg s.c.), both drugs, or vehicle. Rats were then inoculated intravenously with non-immunogenic syngeneic MADB106 cells, and 24 h later lung tumor retention was assessed, or 3 weeks later lung metastases were counted. Additionally, 12 h after surgery we harvested MP-NK cells and circulating-NK cells and compared their numbers and cytotoxicity against MADB106 cells and standard YAC-1 target cells. Surgery significantly increased MADB106 metastasis. Nadolol and indomethacin reduced this effect by approximately 50% when used alone, and significantly more (75%) when used together. Only MP-leukocytes exhibited NK cytotoxicity against MADB106 cells. Surgery markedly suppressed it, and nadolol and indomethacin additively restored it. Similar effects were observed assessing MP-NK and circulating-NK cytotoxicity against YAC-1 target cells. Alterations in the numbers of NK cells were partly associated with alterations in total MP-NK activity, but not with circulating-NK activity. Last, administrating nai ve rats with physiologically relevant doses of a beta-adrenergic agonist (Metaproterenol), and/or with PGE2, additively and independently of each other promoted MADB106 metastasis, simulating the effects of surgery. These findings point at potential prophylactic measures in cancer patients undergoing surgery, and suggest a role for MP-NK cells in resisting metastasis of apparently insensitive tumors.

  • marginating pulmonary nk activity and resistance to experimental tumor metastasis suppression by surgery and the prophylactic use of a β adrenergic antagonist and a prostaglandin synthesis inhibitor
    Brain Behavior and Immunity, 2005
    Co-Authors: Rivka Melamed, Ella Rosenne, Keren Shakhar, Yossi Schwartz, Naphtali Abudarham, Shamgar Beneliyahu
    Abstract:

    Abstract Surgery is imperative for cancer treatment, but was suggested to suppress immunity and facilitate metastasis. Here we study the involvement of catecholamines and prostaglandins (PG) in such outcomes, and the role played by marginating-pulmonary (MP)-NK cells in controlling MADB106 metastasis. Non-operated and laparotomized F344 rats were injected postoperatively with a PG synthesis inhibitor (indomethacin, 4 mg/kg i.p.), a β-blocker (nadolol, 0.6 mg/kg s.c.), both drugs, or vehicle. Rats were then inoculated intravenously with non-immunogenic syngeneic MADB106 cells, and 24 h later lung tumor retention was assessed, or 3 weeks later lung metastases were counted. Additionally, 12 h after surgery we harvested MP-NK cells and circulating-NK cells and compared their numbers and cytotoxicity against MADB106 cells and standard YAC-1 target cells. Surgery significantly increased MADB106 metastasis. Nadolol and indomethacin reduced this effect by approximately 50% when used alone, and significantly more (75%) when used together. Only MP-leukocytes exhibited NK cytotoxicity against MADB106 cells. Surgery markedly suppressed it, and nadolol and indomethacin additively restored it. Similar effects were observed assessing MP-NK and circulating-NK cytotoxicity against YAC-1 target cells. Alterations in the numbers of NK cells were partly associated with alterations in total MP-NK activity, but not with circulating-NK activity. Last, administrating nai¨ve rats with physiologically relevant doses of a β-adrenergic agonist (Metaproterenol), and/or with PGE2, additively and independently of each other promoted MADB106 metastasis, simulating the effects of surgery. These findings point at potential prophylactic measures in cancer patients undergoing surgery, and suggest a role for MP-NK cells in resisting metastasis of apparently insensitive tumors.

  • in vivo beta adrenergic stimulation suppresses natural killer activity and compromises resistance to tumor metastasis in rats
    Journal of Immunology, 1998
    Co-Authors: Guy Shakhar, Shamgar Beneliyahu
    Abstract:

    The sympathetic nervous system has been implicated in mediating stress-induced alterations in NK cell activity, particularly through stimulation of beta-adrenergic receptors. However, because catecholamines induce time-dependent alterations in the distribution of NK cells, the impact of beta-adrenergic stimulation on individual NK cell cytotoxicity is not clear, nor are its implications regarding host resistance to metastatic spread. To address these issues, we used the beta-adrenergic agonist, Metaproterenol (MP), in F344 rats. The number of blood NK cells doubled within 10 min of MP administration and returned to baseline levels within 1 h. By this time, MP suppressed blood NK activity in a dose-dependent manner. Two beta-adrenergic antagonists, propranolol, which crosses the blood-brain barrier, and nadolol, which does not, blocked this suppression. Corresponding findings were obtained using an NK-sensitive tumor model, the MADB106. MP caused an up to 10 times increase in the number of tumor cells retained in the lungs 1 day after inoculation and a similar rise in the number of consequent lung metastases detected 3 wk later. These effects were dose dependent and nadolol reversible. NK cells appear to play a central role in mediating the tumor-enhancing effects of MP because their selective depletion nearly abolished this effect. Overall, our findings suggest that independent of the transitory increase in numbers of blood NK cells, in vivo beta-adrenergic stimulation suppresses NK activity in the rat. This suppression is induced peripherally and can compromise host resistance to NK-sensitive tumors. Homologies to studies in humans and clinical relevance are discussed.

  • in vivo beta adrenergic stimulation suppresses natural killer activity and compromises resistance to tumor metastasis in rats
    Journal of Immunology, 1998
    Co-Authors: Guy Shakhar, Shamgar Beneliyahu
    Abstract:

    The sympathetic nervous system has been implicated in mediating stress-induced alterations in NK cell activity, particularly through stimulation of β-adrenergic receptors. However, because catecholamines induce time-dependent alterations in the distribution of NK cells, the impact of β-adrenergic stimulation on individual NK cell cytotoxicity is not clear, nor are its implications regarding host resistance to metastatic spread. To address these issues, we used the β-adrenergic agonist, Metaproterenol (MP), in F344 rats. The number of blood NK cells doubled within 10 min of MP administration and returned to baseline levels within 1 h. By this time, MP suppressed blood NK activity in a dose-dependent manner. Two β-adrenergic antagonists, propranolol, which crosses the blood-brain barrier, and nadolol, which does not, blocked this suppression. Corresponding findings were obtained using an NK-sensitive tumor model, the MADB106. MP caused an up to 10 times increase in the number of tumor cells retained in the lungs 1 day after inoculation and a similar rise in the number of consequent lung metastases detected 3 wk later. These effects were dose dependent and nadolol reversible. NK cells appear to play a central role in mediating the tumor-enhancing effects of MP because their selective depletion nearly abolished this effect. Overall, our findings suggest that independent of the transitory increase in numbers of blood NK cells, in vivo β-adrenergic stimulation suppresses NK activity in the rat. This suppression is induced peripherally and can compromise host resistance to NK-sensitive tumors. Homologies to studies in humans and clinical relevance are discussed.

Guy Shakhar - One of the best experts on this subject based on the ideXlab platform.

  • in vivo beta adrenergic stimulation suppresses natural killer activity and compromises resistance to tumor metastasis in rats
    Journal of Immunology, 1998
    Co-Authors: Guy Shakhar, Shamgar Beneliyahu
    Abstract:

    The sympathetic nervous system has been implicated in mediating stress-induced alterations in NK cell activity, particularly through stimulation of beta-adrenergic receptors. However, because catecholamines induce time-dependent alterations in the distribution of NK cells, the impact of beta-adrenergic stimulation on individual NK cell cytotoxicity is not clear, nor are its implications regarding host resistance to metastatic spread. To address these issues, we used the beta-adrenergic agonist, Metaproterenol (MP), in F344 rats. The number of blood NK cells doubled within 10 min of MP administration and returned to baseline levels within 1 h. By this time, MP suppressed blood NK activity in a dose-dependent manner. Two beta-adrenergic antagonists, propranolol, which crosses the blood-brain barrier, and nadolol, which does not, blocked this suppression. Corresponding findings were obtained using an NK-sensitive tumor model, the MADB106. MP caused an up to 10 times increase in the number of tumor cells retained in the lungs 1 day after inoculation and a similar rise in the number of consequent lung metastases detected 3 wk later. These effects were dose dependent and nadolol reversible. NK cells appear to play a central role in mediating the tumor-enhancing effects of MP because their selective depletion nearly abolished this effect. Overall, our findings suggest that independent of the transitory increase in numbers of blood NK cells, in vivo beta-adrenergic stimulation suppresses NK activity in the rat. This suppression is induced peripherally and can compromise host resistance to NK-sensitive tumors. Homologies to studies in humans and clinical relevance are discussed.

  • in vivo beta adrenergic stimulation suppresses natural killer activity and compromises resistance to tumor metastasis in rats
    Journal of Immunology, 1998
    Co-Authors: Guy Shakhar, Shamgar Beneliyahu
    Abstract:

    The sympathetic nervous system has been implicated in mediating stress-induced alterations in NK cell activity, particularly through stimulation of β-adrenergic receptors. However, because catecholamines induce time-dependent alterations in the distribution of NK cells, the impact of β-adrenergic stimulation on individual NK cell cytotoxicity is not clear, nor are its implications regarding host resistance to metastatic spread. To address these issues, we used the β-adrenergic agonist, Metaproterenol (MP), in F344 rats. The number of blood NK cells doubled within 10 min of MP administration and returned to baseline levels within 1 h. By this time, MP suppressed blood NK activity in a dose-dependent manner. Two β-adrenergic antagonists, propranolol, which crosses the blood-brain barrier, and nadolol, which does not, blocked this suppression. Corresponding findings were obtained using an NK-sensitive tumor model, the MADB106. MP caused an up to 10 times increase in the number of tumor cells retained in the lungs 1 day after inoculation and a similar rise in the number of consequent lung metastases detected 3 wk later. These effects were dose dependent and nadolol reversible. NK cells appear to play a central role in mediating the tumor-enhancing effects of MP because their selective depletion nearly abolished this effect. Overall, our findings suggest that independent of the transitory increase in numbers of blood NK cells, in vivo β-adrenergic stimulation suppresses NK activity in the rat. This suppression is induced peripherally and can compromise host resistance to NK-sensitive tumors. Homologies to studies in humans and clinical relevance are discussed.

Estrada Solorio, Maria Ines - One of the best experts on this subject based on the ideXlab platform.

  • Eefecto de los uteroinhibidores en la flujometria doppler uteroplacentaria y fetal durante la amenaza de parto pretermino
    'Universitat Autonoma de Barcelona', 2012
    Co-Authors: Estrada Solorio, Maria Ines
    Abstract:

    INTRODUCCION El parto pretérmino es una de las principales causas de morbi-mortalidad neonatal. En el Hospital Civil de Guadalajara, en el año 2008 de un total de 8,896 nacimientos, se reporta un porcentaje de recién nacidos prematuros del 7.9% Los uteroinhibidores como un mecanismo para evitar los partos pretérmino han sido utilizados ampliamente en Obstetricia. Suelen tener una serie de efectos colaterales conocidos en la madre, sin embargo se ha estudiado poco el efecto de estos fármacos sobre el feto. El estudio Doppler pretende obtener más conocimientos sobre las repercusiones en ambos. Lamentablemente no se cuenta hasta hoy con valoración amplia sobre el uso de la Orciprenalina y Nifedipina y la respuesta en la flujometría Doppler de la arteria uterina, arteria umbilical, arteria cerebral media y en el índice cerebro-placentario, tema que genera un gran interés ya que de esta forma se valorarían mejor sus consecuencias durante el manejo de la amenaza del parto pretérmino, siendo que en nuestro medio estos fármacos son ampliamente utilizados para este fin. OBJETIVO PRINCIPAL Valorar la influencia de distintos fármacos útero-inhibidores sobre la circulación materna y fetal valorada mediante estudio Doppler. MATERIAL Y METODOS Se realizó un estudio tipo quasiexperimental, en la Unidad de Medicina Materno Fetal (UMMF) del Hospital Civil de Guadalajara UdeG México. A 27 pacientes se les aplico Orciprenalina y a otro grupo de 27 pacientes Nifedipina con embarazos de 28-34 semanas. Se utilizo el Protocolo de manejo de la UMMF. En ambos grupos se evaluaron los efectos hemodinámicos que pudieran presentarse en la madre y el feto ante su administración. RESULTADOS De un total de 54 pacientes se encontró que a mayor edad gestacional menor el índice de pulsatilidad (IP) cuando fue utilizada la Nifedipina y la Orciprenalina. Los cambios hemodinámicos en los diferentes vasos sanguíneos estudiados mediante la valoración de flujometría Doppler los índices de pulsatilidad (IP) sufrieron algunas variaciones mostrando valores estadísticamente significativos, pero sin salir de los percentiles de normalidad para cada edad gestacional y sin ninguna repercusión en la respuesta clínica materna o en el resultado perinatal. CONCLUSIONES La respuesta hemodinamica materno-fetal evaluada mediante flujometría Doppler en las arterias uterinas (Aut), arteria umbilical (AU), arteria cerebral media (ACM) y el índice cerebro-placentario (ICP) no fuueron afectadas por la utilización de Orciprenalina y Nifedipina durante la amenaza de parto pretérmino.INTRODUCTION Preterm birth is a major cause of neonatal morbidity and mortality. In the Civil Hospital of Guadalajara, in 2008 a total of 8.896 births, reported a percentage of premature infants of 7.9% The uteroinhibidores as a mechanism to prevent preterm births have been widely used in obstetrics. They usually have a number of known side effects in the mother, but has been little studied the effect of these drugs on the fetus. The Doppler study aims to gain more knowledge on the impact on both. Unfortunately there is no comprehensive assessment to date with the use of Metaproterenol and Nifedipine and response Doppler flowmetry of the uterine artery, umbilical artery, middle cerebral artery and cerebro-placental index, a topic that generates a lot of interest and that in this way would be valued best consequences for the management of preterm labor threat, considering that in our midst these drugs are widely used for this purpose. OBJECTIVE To evaluate the influence of different drugs on the uterus-inhibiting maternal and fetal circulation assessed by Doppler study. MATERIAL AND METHODS A study quasiexperimental type in the Maternal Fetal Medicine Unit (UMMF) of the Civil Hospital of Guadalajara Mexico UdeG. A 27 patients received Metaproterenol and another group of 27 patients with pregnancy Nifedipine 28-34 weeks. We used the Protocol UMMF management. Both groups evaluated the hemodynamic effects that may occur in the mother and fetus before its administration. RESULTS Of a total of 54 patients found that higher gestational age less pulsatility index (PI) was used as nifedipine and Metaproterenol. Hemodynamic changes in different blood vessels studied by assessing Doppler flowmetry pulsatility indices (PI) were some variations showing statistical significance, but without leaving the normal percentiles for each gestational age and without any impact on clinical response maternal or perinatal outcome. CONCLUSIONS The maternal-fetal hemodynamic response assessed by Doppler flowmetry in the uterine arteries (Aut), umbilical artery (UA), middle cerebral artery (MCA) and cerebro-placental index (PCI) fuueron not affected by the use of Metaproterenol and Nifedipine during preterm labor

  • Eefecto de los uteroinhibidores en la flujometria doppler uteroplacentaria y fetal durante la amenaza de parto pretermino /
    2012
    Co-Authors: Estrada Solorio, Maria Ines, Universitat Autònoma De Barcelona. Departament De Periodisme I De Ciènc
    Abstract:

    Introducción: el parto pretérmino es una de las principales causas de morbi-mortalidad neonatal. En el Hospital Civil de Guadalajara, en el año 2008, de un total de 8,896 nacimientos, se reporta un porcentaje de recién nacidos prematuros del 7.9%. Los uteroinhibidores, como un mecanismo para evitar los partos pretérmino, han sido utilizados ampliamente en Obstetricia. Suelen tener una serie de efectos colaterales conocidos en la madre, sin embargo se ha estudiado poco el efecto de estos fármacos sobre el feto. El estudio Doppler pretende obtener más conocimientos sobre las repercusiones en ambos. Lamentablemente no se cuenta hasta hoy con valoración amplia sobre el uso de la Orciprenalina y Nifedipina y la respuesta en la flujometría Doppler de la arteria uterina, arteria umbilical, arteria cerebral media y en el índice cerebro-placentario, tema que genera un gran interés ya que de esta forma se valorarían mejor sus consecuencias durante el manejo de la amenaza del parto pretérmino, siendo que en nuestro medio estos fármacos son ampliamente utilizados para este fin. Objetivo principal: valorar la influencia de distintos fármacos útero-inhibidores sobre la circulación materna y fetal valorada mediante estudio Doppler. Material y métodos: se realizó un estudio tipo quasiexperimental, en la Unidad de Medicina Materno Fetal (U03F) del Hospital Civil de Guadalajara UdeG México. A 27 pacientes se les aplicó Orciprenalina y a otro grupo de 27 pacientes Nifedipina con embarazos de 28-34 semanas. Se utilizó el Protocolo de manejo de la U03F. En ambos grupos se evaluaron los efectos hemodinámicos que pudieran presentarse en la madre y el feto ante su administración. Resultados: de un total de 54 pacientes se encontró que a mayor edad gestacional menor el índice de pulsatilidad (IP) cuando fue utilizada la Nifedipina y la Orciprenalina. Los cambios hemodinámicos en los diferentes vasos sanguíneos estudiados mediante la valoración de flujometría Doppler. Los índices de pulsatilidad (IP) sufrieron algunas variaciones mostrando valores estadísticamente significativos, pero sin salir de los percentiles de normalidad para cada edad gestacional y sin ninguna repercusión en la respuesta clínica materna o en el resultado perinatal. Conclusiones: la respuesta hemodinamica materno-fetal evaluada mediante flujometría Doppler en las arterias uterinas (Aut), arteria umbilical (AU), arteria cerebral media (ACM) y el índice cerebro-placentario (ICP) no fueron afectadas por la utilización de Orciprenalina y Nifedipina durante la amenaza de parto pretérminoINTRODUCCION El parto pretérmino es una de las principales causas de morbi-mortalidad neonatal. En el Hospital Civil de Guadalajara, en el año 2008 de un total de 8,896 nacimientos, se reporta un porcentaje de recién nacidos prematuros del 7.9% Los uteroinhibidores como un mecanismo para evitar los partos pretérmino han sido utilizados ampliamente en Obstetricia. Suelen tener una serie de efectos colaterales conocidos en la madre, sin embargo se ha estudiado poco el efecto de estos fármacos sobre el feto. El estudio Doppler pretende obtener más conocimientos sobre las repercusiones en ambos. Lamentablemente no se cuenta hasta hoy con valoración amplia sobre el uso de la Orciprenalina y Nifedipina y la respuesta en la flujometría Doppler de la arteria uterina, arteria umbilical, arteria cerebral media y en el índice cerebro-placentario, tema que genera un gran interés ya que de esta forma se valorarían mejor sus consecuencias durante el manejo de la amenaza del parto pretérmino, siendo que en nuestro medio estos fármacos son ampliamente utilizados para este fin. OBJETIVO PRINCIPAL Valorar la influencia de distintos fármacos útero-inhibidores sobre la circulación materna y fetal valorada mediante estudio Doppler. MATERIAL Y METODOS Se realizó un estudio tipo quasiexperimental, en la Unidad de Medicina Materno Fetal (UMMF) del Hospital Civil de Guadalajara UdeG México. A 27 pacientes se les aplico Orciprenalina y a otro grupo de 27 pacientes Nifedipina con embarazos de 28-34 semanas. Se utilizo el Protocolo de manejo de la UMMF. En ambos grupos se evaluaron los efectos hemodinámicos que pudieran presentarse en la madre y el feto ante su administración. RESULTADOS De un total de 54 pacientes se encontró que a mayor edad gestacional menor el índice de pulsatilidad (IP) cuando fue utilizada la Nifedipina y la Orciprenalina. Los cambios hemodinámicos en los diferentes vasos sanguíneos estudiados mediante la valoración de flujometría Doppler los índices de pulsatilidad (IP) sufrieron algunas variaciones mostrando valores estadísticamente significativos, pero sin salir de los percentiles de normalidad para cada edad gestacional y sin ninguna repercusión en la respuesta clínica materna o en el resultado perinatal. CONCLUSIONES La respuesta hemodinamica materno-fetal evaluada mediante flujometría Doppler en las arterias uterinas (Aut), arteria umbilical (AU), arteria cerebral media (ACM) y el índice cerebro-placentario (ICP) no fuueron afectadas por la utilización de Orciprenalina y Nifedipina durante la amenaza de parto pretérmino.INTRODUCTION Preterm birth is a major cause of neonatal morbidity and mortality. In the Civil Hospital of Guadalajara, in 2008 a total of 8.896 births, reported a percentage of premature infants of 7.9% The uteroinhibidores as a mechanism to prevent preterm births have been widely used in obstetrics. They usually have a number of known side effects in the mother, but has been little studied the effect of these drugs on the fetus. The Doppler study aims to gain more knowledge on the impact on both. Unfortunately there is no comprehensive assessment to date with the use of Metaproterenol and Nifedipine and response Doppler flowmetry of the uterine artery, umbilical artery, middle cerebral artery and cerebro-placental index, a topic that generates a lot of interest and that in this way would be valued best consequences for the management of preterm labor threat, considering that in our midst these drugs are widely used for this purpose. OBJECTIVE To evaluate the influence of different drugs on the uterus-inhibiting maternal and fetal circulation assessed by Doppler study. MATERIAL AND METHODS A study quasiexperimental type in the Maternal Fetal Medicine Unit (UMMF) of the Civil Hospital of Guadalajara Mexico UdeG. A 27 patients received Metaproterenol and another group of 27 patients with pregnancy Nifedipine 28-34 weeks. We used the Protocol UMMF management. Both groups evaluated the hemodynamic effects that may occur in the mother and fetus before its administration. RESULTS Of a total of 54 patients found that higher gestational age less pulsatility index (PI) was used as nifedipine and Metaproterenol. Hemodynamic changes in different blood vessels studied by assessing Doppler flowmetry pulsatility indices (PI) were some variations showing statistical significance, but without leaving the normal percentiles for each gestational age and without any impact on clinical response maternal or perinatal outcome. CONCLUSIONS The maternal-fetal hemodynamic response assessed by Doppler flowmetry in the uterine arteries (Aut), umbilical artery (UA), middle cerebral artery (MCA) and cerebro-placental index (PCI) fuueron not affected by the use of Metaproterenol and Nifedipine during preterm labor

Rivka Melamed - One of the best experts on this subject based on the ideXlab platform.

  • marginating pulmonary nk activity and resistance to experimental tumor metastasis suppression by surgery and the prophylactic use of a β adrenergic antagonist and a prostaglandin synthesis inhibitor
    Brain Behavior and Immunity, 2005
    Co-Authors: Rivka Melamed, Ella Rosenne, Keren Shakhar, Yossi Schwartz, Naphtali Abudarham, Shamgar Beneliyahu
    Abstract:

    Surgery is imperative for cancer treatment, but was suggested to suppress immunity and facilitate metastasis. Here we study the involvement of catecholamines and prostaglandins (PG) in such outcomes, and the role played by marginating-pulmonary (MP)-NK cells in controlling MADB106 metastasis. Non-operated and laparotomized F344 rats were injected postoperatively with a PG synthesis inhibitor (indomethacin, 4 mg/kg i.p.), a beta-blocker (nadolol, 0.6 mg/kg s.c.), both drugs, or vehicle. Rats were then inoculated intravenously with non-immunogenic syngeneic MADB106 cells, and 24 h later lung tumor retention was assessed, or 3 weeks later lung metastases were counted. Additionally, 12 h after surgery we harvested MP-NK cells and circulating-NK cells and compared their numbers and cytotoxicity against MADB106 cells and standard YAC-1 target cells. Surgery significantly increased MADB106 metastasis. Nadolol and indomethacin reduced this effect by approximately 50% when used alone, and significantly more (75%) when used together. Only MP-leukocytes exhibited NK cytotoxicity against MADB106 cells. Surgery markedly suppressed it, and nadolol and indomethacin additively restored it. Similar effects were observed assessing MP-NK and circulating-NK cytotoxicity against YAC-1 target cells. Alterations in the numbers of NK cells were partly associated with alterations in total MP-NK activity, but not with circulating-NK activity. Last, administrating nai ve rats with physiologically relevant doses of a beta-adrenergic agonist (Metaproterenol), and/or with PGE2, additively and independently of each other promoted MADB106 metastasis, simulating the effects of surgery. These findings point at potential prophylactic measures in cancer patients undergoing surgery, and suggest a role for MP-NK cells in resisting metastasis of apparently insensitive tumors.

  • marginating pulmonary nk activity and resistance to experimental tumor metastasis suppression by surgery and the prophylactic use of a β adrenergic antagonist and a prostaglandin synthesis inhibitor
    Brain Behavior and Immunity, 2005
    Co-Authors: Rivka Melamed, Ella Rosenne, Keren Shakhar, Yossi Schwartz, Naphtali Abudarham, Shamgar Beneliyahu
    Abstract:

    Abstract Surgery is imperative for cancer treatment, but was suggested to suppress immunity and facilitate metastasis. Here we study the involvement of catecholamines and prostaglandins (PG) in such outcomes, and the role played by marginating-pulmonary (MP)-NK cells in controlling MADB106 metastasis. Non-operated and laparotomized F344 rats were injected postoperatively with a PG synthesis inhibitor (indomethacin, 4 mg/kg i.p.), a β-blocker (nadolol, 0.6 mg/kg s.c.), both drugs, or vehicle. Rats were then inoculated intravenously with non-immunogenic syngeneic MADB106 cells, and 24 h later lung tumor retention was assessed, or 3 weeks later lung metastases were counted. Additionally, 12 h after surgery we harvested MP-NK cells and circulating-NK cells and compared their numbers and cytotoxicity against MADB106 cells and standard YAC-1 target cells. Surgery significantly increased MADB106 metastasis. Nadolol and indomethacin reduced this effect by approximately 50% when used alone, and significantly more (75%) when used together. Only MP-leukocytes exhibited NK cytotoxicity against MADB106 cells. Surgery markedly suppressed it, and nadolol and indomethacin additively restored it. Similar effects were observed assessing MP-NK and circulating-NK cytotoxicity against YAC-1 target cells. Alterations in the numbers of NK cells were partly associated with alterations in total MP-NK activity, but not with circulating-NK activity. Last, administrating nai¨ve rats with physiologically relevant doses of a β-adrenergic agonist (Metaproterenol), and/or with PGE2, additively and independently of each other promoted MADB106 metastasis, simulating the effects of surgery. These findings point at potential prophylactic measures in cancer patients undergoing surgery, and suggest a role for MP-NK cells in resisting metastasis of apparently insensitive tumors.

Keren Shakhar - One of the best experts on this subject based on the ideXlab platform.

  • marginating pulmonary nk activity and resistance to experimental tumor metastasis suppression by surgery and the prophylactic use of a β adrenergic antagonist and a prostaglandin synthesis inhibitor
    Brain Behavior and Immunity, 2005
    Co-Authors: Rivka Melamed, Ella Rosenne, Keren Shakhar, Yossi Schwartz, Naphtali Abudarham, Shamgar Beneliyahu
    Abstract:

    Surgery is imperative for cancer treatment, but was suggested to suppress immunity and facilitate metastasis. Here we study the involvement of catecholamines and prostaglandins (PG) in such outcomes, and the role played by marginating-pulmonary (MP)-NK cells in controlling MADB106 metastasis. Non-operated and laparotomized F344 rats were injected postoperatively with a PG synthesis inhibitor (indomethacin, 4 mg/kg i.p.), a beta-blocker (nadolol, 0.6 mg/kg s.c.), both drugs, or vehicle. Rats were then inoculated intravenously with non-immunogenic syngeneic MADB106 cells, and 24 h later lung tumor retention was assessed, or 3 weeks later lung metastases were counted. Additionally, 12 h after surgery we harvested MP-NK cells and circulating-NK cells and compared their numbers and cytotoxicity against MADB106 cells and standard YAC-1 target cells. Surgery significantly increased MADB106 metastasis. Nadolol and indomethacin reduced this effect by approximately 50% when used alone, and significantly more (75%) when used together. Only MP-leukocytes exhibited NK cytotoxicity against MADB106 cells. Surgery markedly suppressed it, and nadolol and indomethacin additively restored it. Similar effects were observed assessing MP-NK and circulating-NK cytotoxicity against YAC-1 target cells. Alterations in the numbers of NK cells were partly associated with alterations in total MP-NK activity, but not with circulating-NK activity. Last, administrating nai ve rats with physiologically relevant doses of a beta-adrenergic agonist (Metaproterenol), and/or with PGE2, additively and independently of each other promoted MADB106 metastasis, simulating the effects of surgery. These findings point at potential prophylactic measures in cancer patients undergoing surgery, and suggest a role for MP-NK cells in resisting metastasis of apparently insensitive tumors.

  • marginating pulmonary nk activity and resistance to experimental tumor metastasis suppression by surgery and the prophylactic use of a β adrenergic antagonist and a prostaglandin synthesis inhibitor
    Brain Behavior and Immunity, 2005
    Co-Authors: Rivka Melamed, Ella Rosenne, Keren Shakhar, Yossi Schwartz, Naphtali Abudarham, Shamgar Beneliyahu
    Abstract:

    Abstract Surgery is imperative for cancer treatment, but was suggested to suppress immunity and facilitate metastasis. Here we study the involvement of catecholamines and prostaglandins (PG) in such outcomes, and the role played by marginating-pulmonary (MP)-NK cells in controlling MADB106 metastasis. Non-operated and laparotomized F344 rats were injected postoperatively with a PG synthesis inhibitor (indomethacin, 4 mg/kg i.p.), a β-blocker (nadolol, 0.6 mg/kg s.c.), both drugs, or vehicle. Rats were then inoculated intravenously with non-immunogenic syngeneic MADB106 cells, and 24 h later lung tumor retention was assessed, or 3 weeks later lung metastases were counted. Additionally, 12 h after surgery we harvested MP-NK cells and circulating-NK cells and compared their numbers and cytotoxicity against MADB106 cells and standard YAC-1 target cells. Surgery significantly increased MADB106 metastasis. Nadolol and indomethacin reduced this effect by approximately 50% when used alone, and significantly more (75%) when used together. Only MP-leukocytes exhibited NK cytotoxicity against MADB106 cells. Surgery markedly suppressed it, and nadolol and indomethacin additively restored it. Similar effects were observed assessing MP-NK and circulating-NK cytotoxicity against YAC-1 target cells. Alterations in the numbers of NK cells were partly associated with alterations in total MP-NK activity, but not with circulating-NK activity. Last, administrating nai¨ve rats with physiologically relevant doses of a β-adrenergic agonist (Metaproterenol), and/or with PGE2, additively and independently of each other promoted MADB106 metastasis, simulating the effects of surgery. These findings point at potential prophylactic measures in cancer patients undergoing surgery, and suggest a role for MP-NK cells in resisting metastasis of apparently insensitive tumors.